Pathology of the stomach

Question 1

Pyloric stenosis

Answer 1

• Hypertrophy of muscular is externa in pylorus creating a palpable mass
• Leads to non-bilious (before ampulae of vater) projectile vomiting in newborn
• 3:1 M

Question 2

Type B chronic gastritis: H. Pylori

Answer 2

• Chronic mucosal inflammation leading to eventual muscle atrophy and metaplasia
• 50% in adults over 50
• Histo: lymphoplasmacytic infiltration in the superficial mucosa of the antrum region (favored site for H pylori)
• PMNs almost always seen in lamina propria and in antral mucous glands
• H pylori may be present on surface mucous
• Reactive lymphoid hyperplasia w/ lymphoid follicle formation common
• Dx requires endoscopy and biopsy, there is a lumpy-bumpy appearance on endoscopy

Question 3

Type A chronic gastritis: autoimmune associated w/ pernicious anemia 1

Answer 3

• Autoimmune chronic gastritis leads to T cell-mediated response to parietal cells
• Destruction of parietal cells results in lack of intrinsic factor and thus vit B12 def (pernicious anemia)
• Can test for intrinsic factor and H+ pump autoAbs, but these are not part of pathogenesis of pernicious anemia (T cell dependent)

Question 4

Type A chronic gastritis: autoimmune associated w/ pernicious anemia 2

Answer 4

• Endoscopically the mucosa looks thin, smooth w/ prominent submucosal vessels
• There may be achlorhydria (failure to secrete HCl)
• Histo: lymphoplasmacytic infiltration of mucosa, around parietal cells w/ decreased parietal cell numbers
• PMNs rarely seen, H pylori absent, fundus and body mostly affected (mucosa thins and predominant mucous cells- intestinal metaplasia)
• Complications: hyperplasia of neuroendocrine cells can lead to carcinoid tumors, increased gastric adenoma risk

Question 5

Acute gastritis

Answer 5

• May be ASx, but is associated w/ mild dyspnia, epigastric pain, N/V, hematemesis and melena
• Mechanism unknown, but some causes include drugs (NSAIDs, smoking, steroids), toxins (ETOH, bile reflux), stress, chemoRx, ischemia/shock, systemic infections, trauma, uremia
• Gross path: diffuse hyperemia w/ multiple small superficial erosions or ulcers
• Histo: surface epithelial injury/erosion, lamina propria hemorrhage
• Ulceration w/ perforation rare (acute gastric ulceration is not precursor to chronic peptic ulcer disease)

Question 6

Menetrier disease (hypertrophic gastritis)

Answer 6

• Rare and unknown cause, Dx made by endoscopy
• Overproduction of gastric mucous can lead to increased protein loss in intestine
• Can be associated w/ hypo/achlohydria
• Gross: large rugal folds, may have many polyps
• Histo: hyperplasia and cystic dilation of mucous glands, w/ SmM proliferation in muscularis mucosae
• DDx: malignant lymphoma, gastric CA, zollinger-ellison, eosinophilic gastroenteritis

Question 7

Chronic peptic ulcer disease (PUD) 1

Answer 7

• Ulcer: a defect that extends thru the mucosa and muscular is mucosae into submucosa or deeper at any point of GI tract that is exposed to gastric acid
• Largest risk factor: H pylori gastritis (10x higher)
• Gross: usually solitary, large (>1cm) round/oval lesion w/ punched-out appearance and mucosal folds radiating out of ulcer (may look like CA ulcer, but CA ulcers do not have radiating rural folds)
• Located often in lesser curvature, btwn body and antrum, or 1st part of duodenum (most common site)
• Histo: ulcer base has necrotic debris w/ underlying acute inflammation and granulation tissue deep to inflammation
• Chronic ulcers have extensive fibrosis deep to granulation tissue (often in muscular wall)
• Epithelium at leading edge of ulcer shows inflammatory repair changes and edema
• Must biopsy to rule out CA

Question 8

Chronic peptic ulcer disease (PUD) 2

Answer 8

• Complications: bleeding and Fe def anemia
• Erosion into large vessel: hematemesis or melena (10% of deaths from hemorrhage)
• Perforation: results in chemical peritonitis (rigid abdomen) w/ sudden onset of ab pain and rigidity (70% of deaths)
• Pyloric obstruction: fibrosis around pyloric outlet can lead to severe vomiting
• Penetration: full-thickness ulceration into adjacent organs (no perforation into peritoneal cavity b/c ulceration is slow)

Question 9

Benign neoplasm: mucosal polyps

Answer 9

• Hyperplastic polyps (>80%): lamnia propria is inflamed w/ hyperplastic reactive changes of gastric pits (serrated pits, cysts, edema, abundant apical mucin)
• Fundic gland polyps: hamartomas characterized by normal gastric mucosa w/ cystically-dilated gastric glands lined by chief and parietal or mucous neck cells
• Adenomatous polyps: true neoplasm, moderate risk of carcinoma
• When CA does appear it rarely appears in polyp, but rather adjacent to polyp

Question 10

Gastric adenoCA 1

Answer 10

• Most common stomach malignancy
• Risk factors: chronic gastritis (A or B), adenomatous polyps, dietary nitrites/salt, smoked/pickled foods, foods lacking antioxidants
• There is a diffuse variant (common in youth) associated w/ mutation in e-cadherin characterized by fibrous or mucoid stroma btwn groups of infiltrating cells
• Location: most common is antrum (>50%), cardiac (25%), fundus/body (15-25%) w/ predilection for lesser curvature over greater curvature
• May be early (CA restricted to mucosa and submucosa) or late (CA has invaded the muscular is externa)
• Late is usually when Dx, has various growth types: fun gating, raised-edge ulcer, excavated ulcer (looks like PUD), diffusely infiltrating

Question 11

Gastric adenoCA 2

Answer 11

• Histo for intestinal adenoCA (well-differentiated): well-formed glandular pattern, may have solid or papillary areas (not major component)
• Cells are columnar w/ basal nuclei and no intracytoplasmic mucin
• Spread: to adjacent organs via surface, omentum, peritoneal cavity, lymph (most often to left supraclavicular LN), hematogenous (to lung and liver)
• Clinical (no Sx until later stages): anorexia, anemia, weight loss, hematemesis, melena
• Must be differentiated from PUD by biopsy
• Poor prognosis for advanced gastric adenoCAs (once it invades muscular is externa)

Question 12

Malignant lymphoma of the stomach 1

Answer 12

• Lymphoma presenting in GI tract w/o involvement of liver, spleen or LNs
• 2 most common types: low-grade lymphoma arising in MALT (MALToma) and higher-grade large B cell lymphoma
• MALToma: restricted to stomach, cured by surgical resection
• Can be caused by H pylori
• Clinically similar to PUD and gastritis
• Endoscopically there is lumpy bumpy appearance, usually limited to distal half of stomach
• Histo: destruction of normal glandular or muscular architecture by monocytoid B cells

Question 13

Malignant lymphoma of the stomach 2

Answer 13

• High-grade B cell lymphoma: >50 w/ PUD-like Sxs, also usually restricted to distal half, often a large palpable mass
• Gross: diffuse thickened mucosal folds, polypoid masses, large intramural masses
• Histo: monomorphous population of large non-cleaved lymphocytes arranged in sheets outside of germinal centers, may see eosinophilic infiltrate
• There is infiltration of lamina propria which spreads apart and ultimately destroys the gastric glands (eventually invades muscularis externa)

Question 14

Malignant gastrointestinal stromal tumor (GISTs)

Answer 14

• Clinical: bleeding (hematemesis, coffee-ground emesis, melena), Fe-def anemia, palpable mass
• Dx w/ CT scan
• Gross: large mass arising from wall protruding into lumen and peritoneum
• Mucosal ulceration and cavitation common, tends to grow w/ pushing border, rather than infiltrating
• Does not met to nodes
• Histo: mesenchymal spindle cells w/ high pleomorphism and mitotic activity
• Large tumors show hemorrhage and necrosis
• Stains positive for c-kit and CD34, may express muscle (desmin) and neural (S100) markers